Nassif S, Kempf E, Cardo B, Velley L
Eur J Pharmacol. 1983 Jul 15;91(1):69-76. doi: 10.1016/0014-2999(83)90363-1.
The locus coeruleus of male rats was destroyed bilaterally by injection of 6-hydroxydopamine. Rats injected with the vehicle and normal rats served as controls. Starting 20 days after the lesion, the locomotor activity of all rats was measured for 5 min every day. For the first 6 days, the lesioned rats were significantly less active than control rats; from the 7th to the 15th day, on the other hand, the locomotor activity of the two groups of rats was the same. From the 16th day onwards, the sedative effect of small doses of clonidine (2.5-100 micrograms/kg) was measured in lesioned and control animals. In spite of an almost total loss of noradrenaline in the cerebral cortex and hippocampus and a 33% loss of noradrenaline in the brain-stem of the lesioned rats, the sedative effect of clonidine was the same as in the control rats. This result suggests that the sedation produced by clonidine is not dependent on presynaptically located alpha 2-adrenoceptors.
通过注射6-羟基多巴胺双侧损毁雄性大鼠的蓝斑。注射赋形剂的大鼠和正常大鼠作为对照。在损伤后20天开始，每天测量所有大鼠的运动活动5分钟。在最初的6天里，损伤大鼠的活动明显少于对照大鼠；另一方面，从第7天到第15天，两组大鼠的运动活动相同。从第16天起，在损伤动物和对照动物中测量小剂量可乐定（2.5 - 100微克/千克）的镇静作用。尽管损伤大鼠大脑皮层和海马中的去甲肾上腺素几乎完全丧失，脑干中的去甲肾上腺素丧失33%，但可乐定的镇静作用与对照大鼠相同。这一结果表明，可乐定产生的镇静作用不依赖于突触前定位的α2-肾上腺素能受体。
